Treatment or management of organic acidemias vary; eg see methylmalonic acidemia, propionic acidemia, isovaleric acidemia, and maple syrup urine disease.

As of 1984 there were no effective treatments for all of the conditions, though treatment for some included a limited protein/high carbohydrate diet, intravenous fluids, amino acid substitution, vitamin supplementation, carnitine, induced anabolism, and in some cases, tube-feeding.

As of 1993 ketothiolase deficiency and other OAs were managed by trying to restore biochemical and physiologic homeostasis; common therapies included restricting diet to avoid the precursor amino acids and use of compounds to either dispose of toxic metabolites or increase enzyme activity.

Organic acidemia, also called organic aciduria, is a term used to classify a group of metabolic disorders which disrupt normal amino acid metabolism, particularly branched-chain amino acids, causing a buildup of acids which are usually not present.

The branched-chain amino acids include isoleucine, leucine and valine. Organic acids refer to the amino acids and certain odd-chained fatty acids which are affected by these disorders.

The four main types of organic acidemia are: methylmalonic acidemia, propionic acidemia, isovaleric acidemia, and maple syrup urine disease.

Allergies to a specific pollen are usually associated with OAS reactions to other certain foods. For instance, an allergy to ragweed is associated with OAS reactions to banana, watermelon, cantaloupe, honeydew, zucchini, and cucumber. This does not mean that all sufferers of an allergy to ragweed will experience adverse effects from all or even any of these foods. Reactions may be associated with one type of food, with new reactions to other foods developing later. However, reaction to one or more foods in any given category does not necessarily mean a person is allergic to all foods in that group.

It is unclear what causes alexithymia, though several theories have been proposed.

Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.

French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological at the expense of psychological explanations for the genesis and operation of alexithymia, and introduced the alternative term "disaffectation" to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point "experienced overwhelming emotion that threatened to attack their sense of integrity and identity", to which they applied psychological defenses to pulverize and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word "infans" is from the Latin "not speaking"), and are "by reason of their immaturity inevitably alexithymic". Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be "an extremely arrested and infantile psychic structure". The first language of an infant is nonverbal facial expressions. The parent's emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child's facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent's ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognizing and distinguishing emotional expressions in the child, it can influence the child's capacity to understand emotional expressions.

Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the seretonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.

Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the "equal environments assumption" and the "heritability" estimates in no way correspond to actual DNA structures.

Traumatic brain injury is also implicated in the development alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.

OAS produces symptoms when an affected person eats certain fruits, vegetables, and nuts. Some individuals may only show allergy to only one particular food, and others may show an allergic response to many foods.

Individuals with an allergy to tree pollen may develop OAS to a variety of foods. While the tree pollen allergy has been worked out, the grass pollen is not well understood. Furthermore, some individuals have severe reactions to certain fruits and vegetables that do not fall into any particular allergy category. In recent years, it has also become apparent that when tropical foods initiate OAS, allergy to latex may be the underlying cause.

Because the allergenic proteins associated with OAS are usually destroyed by cooking, most reactions are caused by eating raw foods. The main exceptions to this are celery and nuts, which may cause reactions even after being cooked.

Alexithymia frequently co-occurs with other disorders. Research indicates that alexithymia overlaps with autism spectrum disorders (ASD). In a 2004 study using the TAS-20, 85% of the adults with ASD fell into the impaired category; almost half of the whole group fell into the severely impaired category. Among the adult control, only 17% was impaired; none of them severely. Fitzgerald & Bellgrove pointed out that, "Like alexithymia, Asperger's syndrome is also characterised by core disturbances in speech and language and social relationships". Hill & Berthoz agreed with Fitzgerald & Bellgrove (2006) and in response stated that "there is some form of overlap between alexithymia and ASDs". They also pointed to studies that revealed impaired theory of mind skill in alexithymia, neuroanatomical evidence pointing to a shared etiology and similar social skills deficits. The exact nature of the overlap is uncertain. Alexithymic traits in AS may be linked to clinical depression or anxiety; the mediating factors are unknown and it is possible that alexithymia predisposes to anxiety.

There are many more psychiatric disorders that overlap with alexithymia. One study found that 41% of Vietnam War veterans with post-traumatic stress disorder (PTSD) were alexithymic. Another study found higher levels of alexithymia among Holocaust survivors with PTSD compared to those without. Higher levels of alexithymia among mothers with interpersonal violence-related PTSD were found in one study to have proportionally less caregiving sensitivity. This latter study suggested that when treating adult PTSD patients who are parents, alexithymia should be assessed and addressed also with attention to the parent-child relationship and the child's social-emotional development.

Single study prevalence findings for other disorders include 63% in anorexia nervosa, 56% in bulimia, 45% to 50% in major depressive disorder, 34% in panic disorder, 28% of social phobics, and 50% in substance abusers. Alexithymia is also exhibited by a large proportion of individuals with acquired brain injuries such as stroke or traumatic brain injury.

Alexithymia is correlated with certain personality disorders, substance use disorders, some anxiety disorders, and sexual disorders, as well as certain physical illnesses, such as hypertension, inflammatory bowel disease, and functional dyspepsia. Alexithymia is further linked with disorders such as migraine headaches, lower back pain, irritable bowel syndrome, asthma, nausea, allergies, and fibromyalgia.

An inability to modulate emotions is a possibility in explaining why some people with alexithymia are prone to discharge tension arising from unpleasant emotional states through impulsive acts or compulsive behaviors such as binge eating, substance abuse, perverse sexual behavior, or anorexia nervosa. The failure to regulate emotions cognitively might result in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems which can lead to somatic diseases. People with alexithymia also show a limited ability to experience positive emotions leading Krystal (1988) and Sifneos (1987) to describe many of these individuals as anhedonic.